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Additional info for Developmental biology of neoplastic growth
2002). The few tumors that did develop in Tiam1-null mice exhibited a reduced growth rate compared to Ras-induced tumors in wild-type mice. Furthermore, embryonic fibroblasts isolated from Tiam1-deficient mice had increased apoptotic activity and impaired proliferation, consistent with in vitro studies that implicate Rac1 in tumor formation. Clearly, these data suggest that Tiam1-mediated activation of Rac1 is necessary for Ras-induced transformation. Interestingly, the few tumors that developed in Tiam1-null mice were more aggressive and invasive than those formed in wild-type mice, suggesting that Tiam1 deficiency promotes metastasis of tumor cells.
Cell 100:57–70 Hemmati HD, Nakano I, Lazareff JA, Masterman-Smith M, Geschwind DH, Bronner-Fraser M, Kornblum HI (2003) Cancerous stem cells can arise from pediatric brain tumors. Proc Natl Acad Sci USA 100:15178–15183 Hynes M, Stone DM, Dowd M, Pitts-Meek S, Goddard A, Gurney A, Rosenthal A (1997) Control of cell pattern in the neural tube by the zinc finger transcription factor and oncogene Gli-1. Neuron 19:15–26 Ignatova TN, Kukekov VG, Laywell ED, Suslov ON, Vrionis FD, Steindler DA (2002) Human cortical glial tumors contain neural stem-like cells expressing astroglial and neuronal markers in vitro.
An additional determinant of Rho GTPase function is subcellular localization, which may be influenced by several factors, including post-translational isoprenoid modification and the presence of a C-terminal polybasic region P. Buongiorno, B. ) Development Biology of Neoplastic Growth © Springer-Verlag Berlin Heidelberg 2005 30 Pinella Buongiorno, Bharati Bapat Table 1. Dysregulation of Rho family members in cancer Rho family member Mechanism of dysregulation Tumor RhoA Upregulated RhoB Downregulated RhoC Overexpression Colona, breasta, lunga, testicular germ cellb, head and neck squamous cell carcinomac Head and neck squamous cell carcinomad, lunge Inflammatory breast cancerf,g, pancreatic ductal adenocarcinomah, melanomai RhoA-related Rac1-related Rac1 Rac1b Rac2 Upregulated Hyperactivity Alternative splicing Upregulated Rac3 RhoG Hyperactivity – Breasta Breastj, pancreask, colonk Colon, breastj,l Head and neck squamous cell carcinomac Breastm – Upregulated – – – – – Breasta – – – – – – – – – – – – Gene deletion Downregulated – Breastn Breastn – – Rearrangement – – Non-Hodgkin’s lymphoma, multiple myelomao Diffuse large B-cell lymphomasp Cdc42-related Cdc42 G25K TC10 TCL Wrch-2 Wrch-1 Rnd Rnd1 Rnd2 RhoE/Rnd3 RhoBTB RhoBTB-1 RhoBTB-2 Miro RhoD Rif TTF/RhoH Point mutation aFritz et al.